Abstract
With the rapid increase in the number of blast induced traumatic brain injuries and associated neuropsychological consequences in veterans returning from the operations in Iraq and Afghanistan, the need to better understand the neuropathological sequelae following exposure to an open field blast exposure is still critical. Although a large body of experimental studies have attempted to address these pathological changes using shock tube models of blast injury, studies directed at understanding changes in a gyrencephalic brain exposed to a true open field blast are limited and thus forms the focus of this study. Anesthetized, male Yucatan swine were subjected to forward facing medium blast overpressure (peak side on overpressure 224–332 kPa; n = 7) or high blast overpressure (peak side on overpressure 350–403 kPa; n = 5) by detonating 3.6 kg of composition-4 charge. Sham animals (n = 5) were subjected to all the conditions without blast exposure. After a 3-day survival period, the brain was harvested and sections from the frontal lobes were processed for histological assessment of neuronal injury and glial reactivity changes. Significant neuronal injury in the form of beta amyloid precursor protein immunoreactive zones in the gray and white matter was observed in the frontal lobe sections from both the blast exposure groups. A significant increase in the number of astrocytes and microglia was also observed in the blast exposed sections compared to sham sections. We postulate that the observed acute injury changes may progress to chronic periods after blast and may contribute to short and long-term neuronal degeneration and glial mediated inflammation.
Highlights
Operations Iraqi Freedom (OIF) and Enduring Freedom (OEF) have highlighted the emergence of Blast Induced Neurotrauma (BINT) and the associated mild traumatic brain injury as the signature wound in returning service members [1,2]
Immunoreactive zones in the white matter were associated with stellate-like cells with their dark stained processes surrounded by retraction balls and axons showing signs of swellings (Fig 1I)
This study is the first of its kind to attempt to address the fundamental question whether an open field blast exposure causes injurious changes in the gyrencephalic brain
Summary
Operations Iraqi Freedom (OIF) and Enduring Freedom (OEF) have highlighted the emergence of Blast Induced Neurotrauma (BINT) and the associated mild traumatic brain injury (mTBI) as the signature wound in returning service members [1,2]. Shell shock and post-concussive syndrome had a similar prominence during World Wars I and II [3] With much of these injuries more recently sustained following exposure to an improvised explosive device, basic understanding of the mechanisms and pathological changes in the central nervous system following an open field blast exposure still remains an area of intense research focus. Understanding the pathological changes in the brain following an open field exposure is important considering the complex neurological problems reported in the exposed service members. The history of blast related mTBI has been significantly associated with post-traumatic stress disorder (PTSD) and other physical problems in veterans from OIF [4] as well as those from OEF and Operation New Dawn [5,6]. TBI independent of an injury mechanism (blast or non-blast) has been described as a primary driver of adverse outcomes in an analysis of US military personnel [13]
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